1. Academic Validation
  2. Endoplasmic reticulum-mitochondria coupling attenuates vanadium-induced apoptosis via IP3R in duck renal tubular epithelial cells

Endoplasmic reticulum-mitochondria coupling attenuates vanadium-induced apoptosis via IP3R in duck renal tubular epithelial cells

  • J Inorg Biochem. 2022 Jul;232:111809. doi: 10.1016/j.jinorgbio.2022.111809.
Junjun Peng 1 Chengcheng Peng 2 Li Wang 1 Huabin Cao 1 Chenghong Xing 1 Guyue Li 1 Guoliang Hu 1 Fan Yang 3
Affiliations

Affiliations

  • 1 Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, No. 1101 Zhimin Avenue, Economic and Technological Development District, Nanchang 330045, Jiangxi, PR China.
  • 2 Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, No. 1101 Zhimin Avenue, Economic and Technological Development District, Nanchang 330045, Jiangxi, PR China; Department of Pharmacy, School of Medicine, Guangxi University of Science and Technology, 257 Liu-shi Road, Liuzhou, 545005, Guangxi, PR China.
  • 3 Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, No. 1101 Zhimin Avenue, Economic and Technological Development District, Nanchang 330045, Jiangxi, PR China. Electronic address: yfan@jxau.edu.cn.
Abstract

Vanadium (V) is necessary for the health and growth of Animals, but excessive V has harmful effects on the ecosystem health. Endoplasmic reticulum (ER)-mitochondria coupling as a membrane structure connects the mitochondrial outer membrane with the ER. The mitochondria-associated ER membrane (MAM) is a region of the ER-mitochondria coupling and is essential for normal cell function. Currently, the crosstalk between ER-mitochondrial coupling and Apoptosis in the toxic mechanism of V on duck kidney is still unclear. In this study, duck renal tubular epithelial cells were incubated with different concentrations of sodium metavanadate (NaVO3) and/or inositol triphosphate receptor (IP3R) inhibitor 2-aminoethyl diphenyl borate (2-APB) for 24 h. The results showed that V could significantly increase Lactate Dehydrogenase (LDH) release, the mitochondrial calcium level and the numbers of the fluorescent signal points of IP3R; shortened the length ER-mitochondria coupling and reduced its formation; markedly upregulate the mRNA levels of MAM-related genes and protein levels, causing MAM dysfunction. Additionally, V treatment appeared to upregulate pro-apoptotic genes and downregulate anti-apoptotic genes, followed by cell Apoptosis. The V-induced changes were alleviated by treatment with IP3R inhibitor. In summary, V could induce the dysfunction of ER-mitochondrial coupling and Apoptosis, and inhibition of ER-mitochondrial coupling could attenuate V-induced Apoptosis in duck renal tubular epithelial cells.

Keywords

Apoptosis; Duck; Endoplasmic reticulum-mitochondria coupling; Inositol triphosphate receptor; Renal tubular epithelial cell; Vanadium.

Figures
Products